Ask Me (Almost) Anything With Dr Johnston | Live Q&A

We hit all the high points today! Nutrition, exercise, lipids, dental health, hormones, and more. We had amazing participation and it was wonderful to have a chance to interact with everyone in real time. Thanks SO much for taking some of your precious weekend to talk cardiovascular health, heart scans, CAC scores, and all the other nerdy prevention things with me. Hope you enjoyed it! If you want me to do more of these in the future, please say so in the comments!

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🧬 About Dr. Lily Johnston
  
Dr. Johnston is a double board-certified vascular and general surgeon in San Diego, specializing in metabolic and cardiovascular prevention. She’s the founder of CorSight Health and a passionate advocate for reimagining how medicine approaches chronic disease.

Transcript

SPEAKER_00 0:05

So, how do I know if I have cardiovascular disease? What should I eat to prevent a heart attack or stroke? And what about supplements? What about medications? You guys ask me these questions all the time in the comments, and I am so excited for my first YouTube live Ask Me Anything. We are gonna get it all taken care of. I hope today we are gonna go through all your questions to the best of my ability, and I'm really excited to have you all here with me. If you guys don't know me, my name is Dr. Lily Johnston. I am a board certified vascular surgeon, but I specialize in cardiometabolic prevention. So hopefully you will never need me as a surgeon. All right, guys, thank you so much for being here. We have questions in the anonymous form. We already have questions in the chat, and we're gonna dive right in. So the first question I have: my brother just received a stent. Do I need to tell my MD? I don't want all the scans. I have no symptoms. I'm on Lo Sartin, which is a blood pressure medicine. My LP little A is 24. Thanks. So, you know, my approach to this is it kind of depends on if you don't want scans and you don't want more testing, then I guess you're not obligated to tell your doctor, you know, your doctor works for you. So this is really about what you think you need for your own optimal health and what the differences are between you and your brother. And, you know, that might mean that there's some genetic predisposition in your family to cardiac disease. And perhaps you would want some imaging or perhaps not. I mean, it says you don't want scans. So the question is, you know, what is your MD going to do with this information? What are you gonna do with this information? And, you know, I would ask yourself why you don't want the scans. Um, if you wouldn't change anything, if you're not prepared to make any changes based on that new information in your family, then you know, keep doing what you're doing. Um, if it were me, I might want to be scanned, but that is the difference between a doctor who treats individual patients and takes their own thoughts and feelings into account, and somebody who says, Well, these are the guidelines and we should all just obey them. Um, I know that there are a lot of people who think that it's my job as a doctor to tell you what to do. It is my job to tell you what the data say and what the evidence says. And it's your job to decide what makes sense for you and what your goals are. So that's a really goal-driven question, and you can answer it best, not me. Next, Greg says 73-year-old male, lots of labs, quarter water, quarterly water fasts, and a CAC of 851. What drugs? The goals are LDL 70, uh, or pheno age of 63, CTA, echo, anything else. So um, there are gonna be a number of these, right? I am not your doctor. I am a doctor on YouTube. And what I can tell you is I think the answer to all of these questions about, you know, here are my stats and my numbers, and here are my scores, what do I do? Um, I can't answer those specifically. What I can say is if you have plaque, we need to know why. Or we need to do our best to understand why. Is that a genetic problem? Was that a history of insulin resistance that maybe has gotten better? Is that a history of smoking that you have quit, but it sticks with you? And now we have to sort of mitigate the rest of your residual risk as best we can. Uh, is it an inflammatory problem? Where is the plaque coming from? That is really the next question in my mind. And then how are we going to drive risk, residual risk down? And that answer is gonna be different for everybody. We just don't know exactly, you know, from the surface level, what's driving this? And that is why it takes me an hour or two to go through this with patients and figure out exactly what are we talking about in terms of family history, in terms of nutrition and historical labs, present labs, imaging and functional status, all of these things come together to help me create a personalized plan for people's uh risk reduction because it's just not the same for everybody, no matter how many pages of guidelines we comb through. So, you know, I'm not sure what's next for you. If you want your LDLC under 70, and I think that's a great goal with that elevated CAC. Um, there are a lot of ways to do it, right? Uh, nutrition is one good pillar of this. And once that is at a place where it is sustainable and optimized, as best you can do, then we see where we are and we move on to medications and lipid lowering. I would do my best to avoid uh drugs that are causing you personally side effects, but most people tolerate uh lipid lowering therapy quite well. And if not, great news, there are so many options. So I think you know, all of those are reasonable, but I would take it in the bigger picture and understand what the root cause is first if we can. Sometimes we don't get satisfying answers to that question, but I do think we can do a lot of due diligence to dive into your labs and your history and find out what's going on and really attack that root cause. All right, I'm gonna go to one of the anonymous questions. Do you have any thoughts about microplastics that might be found in bottled water? Is filtering water at home necessary and or preferred over bottled water? So this is a great question, and it speaks to one of the videos I did recently talking about all of the microplastics, like nanoplastics and possibly also the forever chemicals that are maybe contributing to plaque formation. Because we know that if we look at plaques in the arteries in the neck that I take out during a procedure called carotid endarterectomy, we find that patients who have a lot of that microplastic or nanoplastic material in those plaques, yeah, it gets in the plaques, gross. Um, if we look at those patients, they have much higher rates of heart attack and stroke than those who did not have those microplastics. We don't know what that means. Uh, all of us, I think, are trying to avoid those microplastics as best we can, but it seems like it might be playing a role in cardiovascular disease. Now, the microplastics and nanoplastics and forever chemicals are actually everywhere, right? They're in our clothes, they're in our like pods for laundry and dishwashing detergent, they are in the water. Bottled water seems to be particularly bad. Whether your tap water is better or not depends a lot on where you live and what else might be in your water. I was looking at water filters earlier. Um, I'll drop one later in the description uh that does seem to be pretty effective at filtering out microplastics and forever chemicals, but it does nothing for total dissolved solids. And so some people find that, you know, they're trying to like measure the total dissolved solids in their water. You can reduce that and do nothing for the microplastics. Conversely, you can filter out forever chemicals and fluoride and microplastics, but not actually do anything for the total dissolved solids. Some people even report that their total dissolved solids might go up. And so it's really a question of what are you trying to get out of your water? Because there are a number of different contaminants that might be there. And really doing your research and your diligence to find the filter or filtration system that's gonna work best for you. Um, I'm currently renting my apartment, so like I'm not gonna install a huge reverse osmosa system. Uh, I have a countertop filter system that I like, but again, uh I've evolved, right? I originally I started just looking at total dissolved solids and I thought that was enough. And then I looked to see, and I was actually surprised to find that no, it's not actually filtering at any of the microplastics. It's just um making it so that my kettle doesn't scale badly. But uh anyway, that's a long way of saying. I do think you should be cognizant of all of the sources of microplastics in your environment and do what you can to mitigate that. Um, I personally filter my water, and uh, but I live in a place with, you know, pretty dirty is the wrong word, but um, certainly highly mineralized water. And uh I also do worry about those microplastics. But I have no evidence that reducing it will reduce our risk of heart attack and stroke. Just to be very clear about that, there's no evidence yet that any intervention we do for microplastics, including things like buying specialized probiotics with bacteria that absorb plastics in our gut, it gets sounds super cool and maybe it's worthwhile. I just don't know. But we don't yet have any evidence in humans that that's going to reduce our risk. We all hope it will. And if the risks are low for us, then maybe that's a worthwhile thing to do. We just don't know yet. All right, next question. Eve catch all 984 asks a fair amount has been written about estrogen and cardiometabolic health in women. How about men? Is low testosterone an independent vascular risk factor or more a biomarker of poor metabolic health? I love this question. I love talking about hormones. Okay, so yes, estrogen is a cardiometabolic risk factor in women, or the loss of it can uh result in worsening cardiometabolic biomarkers for sure. And it's one of the things I love helping women with as they're in peri- and postmenopause. Um, low testosterone is certainly associated with poor cardiometabolic status. There are a few studies that do show that testosterone replacement therapy to physiologic, not superphysiologic, not Jimbro gear levels, but like physiologic levels can in some studies help reduce the insulin resistance biomarkers, help prevent progression to diabetes. There are other studies that show very little impact. I don't know whether this has to do with the patient population, the dosage at which the testosterone was administered. Um, what I will say is that it's important not to ignore the impact of estrogen in men. We actually don't talk about this enough. And especially in men who are being treated for aggressive prostate cancer with androgen deprivation therapy, that is also by virtue of the fact that the only estrogen in men comes from aromatization of testosterone. It is also estrogen deprivation therapy in men. They get menopause with a mustache, they get hot flashes and night sweats, they get uh excess subcutaneous fat. It's actually not as much visceral fat, which is interesting, anyway. And uh bone loss, osteoporosis, and fracture risk in men. And you can uh safely replace the estrogen without replacing the testosterone. And for some men, this is uh life-changing in terms of their quality of life. So estrogen is also important for men and it's a male hormone. I use testosterone replacement to manage symptoms. Um, I am not as bullish about it as some of my, you know, other colleagues in the sort of lifestyle longevity prevention wellness space. Um people who come to me and ask for it, we can talk about it and I and but I don't push it. I never like go out of my way to suggest it. I'm not sure that I believe in it that strongly as a marker for or as a lever to move the equation for cardiometabolic medicine. But I think if people have low libido, low energy and um are not able to do the things that will, in fact, improve their cardiometabolic status, especially exercise, especially getting out of the house and getting some sunshine and some time out in the big wide world and doing their social connection and doing what drives them to be happy and fulfilled in life. If those things are not working well for whatever reason, I am open to a trial of testosterone replacement to see if that makes any of that better. Uh, but I don't think that by itself it is necessarily driving an improved risk for heart attack, stroke, or diabetes. Um, I'm not the data are not super strong on that. So I hope that answers the question. I think I'll stop there so we can keep going. All right, next anonymous question. Since a lot of cardiovascular diseases can be caused by a person's genetics, at what age should a person start getting genetics testing? This goes back to the idea about, you know, when do you want to know and what are you gonna do about it? So your genetics are your genetics from birth. You could test as early as, you know, getting your kids tested before they even know what any of that means. But if you're not gonna do anything with the results, then you don't need to get tested yet. And I think as much as genetics are absolutely playing a role, it's never the wrong idea to just optimize your nutrition and your exercise and your sleep and your stress because no matter what your genetics are, always that is the foundational approach to helping reduce chances for heart attack and stroke. Now, if you think you have familial hypercholesterolemia, uh getting your lipids checked, you don't even have to get the genetic test for tests for FH or LP little A. You can just get your levels checked and get started on managing that as early in life as you are willing to do it. My approach to this is that, you know, this is all about time under the curve, meaning the earlier we start interventions, the smaller those interventions have to be because our interest compounds over time. It is just like saving for your retirement account. Okay, your cardiovascular health is your body's retirement account. And the earlier you start making deposits for the good, the earlier you get compound interest and the greater the impact of those changes over time. So I see a lot of folks who have come to a health journey in their 40s and 50s. And at that point, it's still an amazing thing to do. I will never argue with it. And we may still have to make some more drastic changes to account for whatever happened in the first 40 to 50 years of life where we were not necessarily as conscientious about our health and well-being. And that is true for all of us. We are all doing the best we can at any given moment. And if you're starting that journey in your 20s and 30s, you're gonna have a lot more going for you by the time you get to 40 or 50 than if you just started your big wellness push at that time. So the answer is get tested as soon as you're ready to act on that information and start making, you know, your your health deposits. All right. Erlen 1665. What are some of your normal everyday diet choices and or the foods that are science-backed for cardiac and vascular health? So my own diet choices are about a lot of things. Of course, they are include, they include what is right for cardiac and vascular health because that's my jam. But I think that my approach to all of this is much broader. And people get confused by this a lot because I don't make the same recommendation across the board. If you have watched my channel for any length of time, if you have seen me on other podcasts, you are probably aware that in general, I tend to skew a little bit towards therapeutic carbohydrate reduction because I see a lot of patients with insulin resistance on diabetes. And it is one of several approaches that is evidence-based and works pretty well. It tends to be the one that is pretty well tolerated and uh is easy for compliance, but it's not the only one that works. I personally don't eat grains and I don't eat a lot of starch because I find that I have a hard time controlling my total energy consumption if I eat those foods. That is not because they're evil. It is just a it's a me thing, and I do find that it's true in many of my patients as well. Um, I am, you know, I've done it all. I have gone low fat, I have been, I've done fasting, I have done carnivore, I have done uh all types of approaches to my own nutrition right now in April of 2026. What is working for me is a lower carb approach, lots of vegetables. I'm trying to increase my soluble fiber intake, and I am trying to stay toward fish and lean meats rather than a lot of the fattier cuts of meats. I'm trying to use olive oil and avocado oil if I'm cooking, um, but I'm not afraid of a little butter. I'm not afraid of a little coconut oil. Also, my cardiac risk may not be what yours is. So we titrate our nutrition to what is going on in our own personal health, what is going on around us. I also am doing a big strength training push right now. I am working really hard to increase my compound lifts. So protein is a big deal for me, and I am working hard to make sure that I am getting an adequate amount of protein to meet my exercise goals. And there are days where, like yesterday, I was in the operating room for about 12 hours. I might not have met those, uh, my protein goals, but I have to figure out how I eat to accommodate that. And so sometimes I will supplement with protein shakes or some other things that are a little bit more processed. They are a little less whole foods than I would optimally like, but that's the reality of my day-to-day life. And I think that encouraging people to achieve a diet that is the way that I eat today is the way I can foresee myself eating for the next five to 10 to 20 years. If you are not eating in a way today where you could sustain this for years, then it's probably not gonna work for you, right? It might be the best diet in the world to lower your LDL cholesterol or to lower your inflammation or to drop weight fast. But if you're not gonna do it forever, what is it, is it helping you, right? Are you are you really helping yourself and the cause? So the best diet for cholesterol reduction is maybe not the best diet for weight loss, is maybe not the best diet for low inflammation or for gut health, is maybe not the best diet for you. This is really deeply personal, and everybody is has different goals. So, again, we can break this down into uh a framework that I have heard used before. It is not mine, but are you um overnourished or adequately nourished, right? Do you have excess body fat to lose or do you have none? And then what is your muscle mass? Because again, above and beyond heart attack and stroke risk, if that's not what gets you, I don't want you to be frail. I don't want you to fall and break a hip because if you're over 70, the mortality rate of a hip fracture is enormous. It's I forget what the exact number is, but like call it 10 to 15%, maybe 50%. It's it's high. It's very, very high for something that ought not, that doesn't sound like it should be fatal. Um, but the issue is people get in the hospital, then they have surgery, then they get a blood clot, or they get an ammonia, or you know, there's a complication from surgery. It's bad. So again, if we're thinking about the bigger picture, just because cardiovascular disease is the leading cause of death in men and women, we're not going to ignore the risks of dementia. We're not going to ignore the risks of falling and breaking a hip. This is the big picture here, right? We don't want to be so laser focused on just one disease. This is all about our complete health and wellness. Clear as mud? Yeah. We should probably do a whole video on nutrition and exercise or sorry, just nutrition uh and the foods and all of that. I will, I am working on that. Uh, it's gonna, you can imagine based on how convoluted that answer was, it's tough for me to nail that down into a quick um quick video, but I'm gonna do my best here. All right. Apo C1 and APOC3, JPAT, thank you. Uh, quest HDL panel, e flux capacity. So, this is all about what is the function of our HDL particles and what are some of the more advanced lipid metrics? What are they telling us? How do we feel about this? I think this is very intellectually interesting from a lipidology nerd standpoint. I am not personally sure that we know how to operationalize any of this or know what recommendations to make if the numbers are not where we want them to be. Um and we are starting to see a lot of drug targets in this space. It's going to be really exciting to figure out what the outcomes look like, what the biomarkers are looking like as we start playing with some of the additional lipid targets. Um, my my gestalt on this is while I enjoy reading about it, and I do think it's very interesting to try to understand the functionality of our HDL. So let me back this up for the non-lipidology nerds. The old idea that HDL high is good is not true. Um, it is low HDL, HDL cholesterol, low HDL cholesterol is associated with metabolic syndrome. And low HDL cholesterol is also typically associated with high triglycerides. Those are two out of the five markers for metabolic syndrome, meaning insulin resistance, and those are absolutely associated with increased risk of heart attack, stroke, adverse cardiac events. We have not shown that increasing HDL improves outcomes. Normal HDL is considered normal, average. It is not necessarily protective, and high HDL cholesterol is sometimes protective in large populations, but sometimes it's also actually a negative thing. And we think that is because it means the HDL is not functioning appropriately. It is not able to engage in reverse cholesterol transport in the normal way. Uh, the particles are getting the cholesterol is getting stuck in that HDL and it's not able to efflux effectively. And so there can be dysfunctional HDL particles. And unlike just measuring the total number of L allele particles, that tells us a lot about your atherogenic risk in a population level. The number of HDL particles by themselves is not actually all that helpful. We don't know what that means. The next evolution is trying to understand how well are those HDL particles working for reverse cholesterol transport? And can we know more about how that process is going based on some of these more advanced testing measures? And I think we're starting to get there, but from a clinical standpoint, I am not sophisticated enough if you Yet to know what to do with those tests or how to change our strategy or our approach clinically based on that information. So I'm not ordering them yet. I'm not really comfortable interpreting them yet. That is interesting from a biohacking and from a lipidology standpoint, but I'm not quite there yet. So stay tuned. Hopefully, in the next few years, we will get to learn more about that and I will be on that journey with you. If you want to teach me more about that, JP, let me know. I'm always excited to hear more about that and learn from you. All right, Harlan, I have PAD in both legs. I have told biovascular doctor that I should not have stents placed because of complications with leg stents. Is that true? PAD, all right, peripheral arterial disease. This is my bread and butter in the hospital side. This is why I hope you guys learn the prevention side, or at least so you never need me. Harlan, if you are somebody who is just having pain with walking, or even better, asymptomatic peripheral arterial disease, yeah, you should probably not make uh plans to get that treated yet with procedures. But if you are at a place where your feet are hurting at night, that's called rest pain, or you have wounds on your feet that aren't healing, that is the beginning of tissue loss, then that is limb threatening. But when we talk about peripheral arterial disease, it is a spectrum. Just like cardiac disease or coronary disease, there are people who have like a positive calcium score, but no chest pain ever. Um, it just happens to be something we see that's asymptomatic. There are people who have stable angina. This is some chest pain or pressure that they get when they're exercising or when they're walking upstairs or with certain activities that goes away. It's been investigated and we've discovered that this is sort of stable disease, and it comes on when the heart needs a little extra oxygen and is not quite able to get as much oxygen as it wants. Then there's unstable angina or heart attacks. Those are different things, but they're on a spectrum, and that is an emergency, right? That is something where we have to resupply the heart with that oxygen and that blood, or else the heart will die, and that's a real problem. So PAD is on that same spectrum. There are people who have PAD that's detected incidentally that have no symptoms. That is actually the ideal scenario because now we can really double down on risk reduction, understanding why you have plaque, where it came from, trying to do everything we can to minimize the chance that the plaque grows and to minimize the chance that you have a plaque rupture event that causes a major problem, like heart attack, stroke, or limb loss. Because if by the way, if you have it in your legs, almost certainly you have it other arteries in your body, like the ones around your heart, like the ones going up to or in your brain. So, whatever we can do to reduce your risk of having any of those cause trouble, we should absolutely do. Claudication is the leg version of stable angina. Claudication is pain with walking. Typically, it is calf muscle cramping, sometimes thigh or buttock muscle cramping. And patients who clearly have vascular cloudication tell me it's the same distance every time, right? It's always the sixth mailbox, or it's always this third hill on my walk, or it's always the second flight of stairs. I get the cramping. If I stop and rest, it gets better and then it goes away. Um, if I start walking again, it comes back, right? This is the cloudication. And if you are a claudicant, then walk, walk, walk and reduce your risks based on why we think you have plaque. But the more you can avoid having a procedure, the longer you will keep your legs and the healthier you will be. Um, stents do not treat this disease, they treat the anatomic narrowing in one little spot. But anytime you put a stent in, there's a risk of bleeding infection, making the circulation worse rather than better, right? Little bits can flick off, the artery can dissect, uh, and the stent can thrombose or immediately clog up with material and blood. So stents are not a freebie. Um they may reduce the pain with walking, but typically speaking, it is not a treatment for the disease. It is just a treatment for the one place where that disease is causing a huge amount of trouble. So stents are a great tool when we are at risk for limb loss. We are uh at a place where the pain in the legs with walking is so bad that you just can't live life reasonably anymore. That is called lifestyle limiting cloudication. Uh, and that is a reasonable time to get your stents done or get your bypass done or get your clean out, whatever the procedure your your surgeon recommends. But I would never think of surgery or stents as a way to treat the disease. It is really a way to treat a very focal area of the disease that is causing you trouble, but you still have plaque everywhere. So the first order of business, particularly if we're not at risk immediately for losing the leg, would be to get your lifestyle under good control, get your risk factors managed, and do every walking or other kinds of exercise that you can to help your body build those collaterals, those extra small blood vessels that get bigger over time and go around the areas that are narrowed or blocked. If you have more questions about PAD, let me know. Hit me up. All right. Let's see. Can I discuss zonulin haptoglobin related to leaky gut and gluten-minimizing diet? Um, short answer, I am not an expert in leaky gut. I personally feel better without gluten in my diet or grains in general, but I am not celiac. I do not have any tested gluten sensitivity. I do think that a lot of the things in our modern processed food environment are inflammatory to our gut and cause the zonulin or the little sort of lock and key mechanism that keeps our intestinal cells tight, right? Basically, the inside of your gut is just like the outside world. It is really a tube, and um everything in that tube is supposed to sort of stay external to the body unless it is helpful and useful to us, at which point we decide to let that in, right? Our nutrients, our protein, all of this, we bring in deliberately. But the bacteria that we eat that are not helpful to us, the pathogens, any of the waste products, right, that should all stay on the inside of the gut and and outside of the body. It's weird to think about it. I need a diagram which I don't have, but um long story short, if your gut gets permeable, meaning stuff starts to filter in that we're not necessarily actively trying to bring into our bodies, uh, that's not optimal. And it tends to cause immune responses that we are not happy about, right? That make us more reactive to things more inflamed. Um, this is a really interesting area of scientific development. I don't think we know nearly as much about it as we say we do. Um, there's just so much diversity in our microbiota. There's it's very difficult to study. The intestinal tract is very long. The pH is very different in different parts of the intestinal tract, and our ability to sample this, right? To have you bring in a sample and understand the millions and billions of different organisms and how they are all working together in the body when they're excreted is very different. So I just don't think that we have quite the level of sophistication and understanding all of this. But if you feel better removing gluten from your diet, by all means, do it. There are people who are able to eliminate it for a brief period of time and actually do a whole elimination diet. This is something that's that's discussed in in other parts of less traditional medicine. And after a while, if you can actually heal the gut, you may be able to reintroduce those foods without too much trouble. Uh, but that's really not my own personal area of expertise, and it's not something that I do a lot of individual coaching on or um discussion in my in my practice. Theodore, will FFRCT eventually replace stress tests? So, what's FFRCT? This is um fractional flow reserve, and this is a way of using a CT scan, a CT angiogram, to help understand whether the narrowing that is in a coronary artery in the heart is causing what we would consider hemodynamically significant stenosis, meaning what is the pressure gradient across that narrowing? And if the drop in pressure from before the narrowing to after the narrowing is significant, and we would say um, you know, like more than 70 or 80 percent tends to be pretty significant, then that might be how we guide the placement of stents in the future. This is potentially more sensitive than a stress test. And a stress test is everything from actually putting you on a treadmill and making you climb, you know, uh do the Bruce protocol on a treadmill test, or people do pharmacologic stress tests. They inject something that makes the heart muscle work really hard and stress it that way. Some people do this with pet imaging, some people do this with an echo or just an EKG. Stress test is all kinds of different ways of making the heart work harder and trying to understand if while the heart is working harder, it seems to be angry, upset, needing more oxygen. I have heard a lot of stories anecdotally, and anecdotes are not data, so I hate to say this, like I'm a little mad at myself for actually bringing this up, but a lot of people have had normal stress tests and gone on to have a heart attack. Um, and I do think that FFRCT is probably a better test. I would say that there's a lot of inertia behind classic stress testing, and a lot of cardiology divisions uh use that as a financial boost for their practice. And so there may or may not be some incentives to stick with classical stress testing. Uh personally, I would rather somebody get a CT angio than a stress test in my practice, but I am not a cardiologist, I don't even play one on television. So take that, take that with a grain of salt. I know cardiologists who do both. Um, some who still recommend stress tests and some who prefer CTA. Uh stay tuned on that one. All right. Oh, we are getting lots of amazing questions here. Okay, um, I'm gonna go back to the anonymous questions. Does having tartar plaque on your teeth indicate that you have plaque in your arteries? In other words, plaque on your teeth, plaque in the arteries, is it the same thing? No, it's not the same thing. However, there is absolutely a link between periodontal disease uh and cardiovascular disease. Right now, at the major society levels, meaning the American Heart Association, American College of Cardiology, it is still considered association, not causation. But there are other groups who feel pretty strongly, like the Baldonine groups, that the treatment of periodontal disease is fundamental to the treatment and reduction of cardiovascular risk. So this is everything from you know getting periodontal pathogen testing to cone beam CTs if you have a root canal and evidence of inflammation to make sure that you don't have a subclinical abscess. And we absolutely see evidence of the pathogens in our mouth also can be found in these plaques in our neck that I scrape out. This is not something we test for routinely, but people have, you know, taken those plaques and studied them under a microscope, and you find pieces of plaque or pieces of these bacteria from our mouth in the plaques in our arteries. And there does really seem to be an association pretty strong between having poor dental health and having increased levels of inflammation, which again drive plaque and drive destabilization of plaque. Uh, my partner in an old practice had a patient who kept having cardiac events and nobody could figure out why until we realized he had like raging infection in his mouth that was untreated. And uh my partner figured that out, treated his infections, and all of a sudden his cardiac situation really stabilized out, and he was able to calm everything down and get that get that patient um moving in a much better direction pretty quickly. But figuring that out was something that took a much broader perspective than the average doctor uh will will have. So that's a great question. And the short answer is they're not the same plaque, but they actually are very much interrelated. All right. Oh, yes. Makita says, so glad I was able to make it. Thank you for making it available. Yeah, you're very welcome. This is a lot of fun for me. Uh all right. Mutant. I have suffered migraines and fogginess for decades. Neurologists tried all kinds of other things. What was recently suggested? 20 milligrams of PQQ twice a day, and it works. Great. I'm glad you found a solution. Uh headaches are chronic headaches are a real problem. Not my area of expertise either. All right. Oh, hives lupus, also not my strength. I'm sorry. When is the best time to test LP little A? Mine has been 81 and then 133. I thought it hardly changes. Thank you. This is an important point. So you have heard me in a video and many others say LP little A is genetically determined and it doesn't change. That's not true, and anybody who's had serial testing will tell you that actually their levels have varied within maybe even as much as 20%, um, up to 40%, depending on when they've tested. There is evidence to support the fact that LPA is partially an acute phase reactant. This means LPA may change during states of high inflammation in the body, whether that's during an illness, an infection, something else. And if we are having high levels of inflammation, LPA may fluctuate quite a bit. Um overall, generally speaking, when we test people serely for LP little A, which by the way is not really recommended, people stay in the same bucket of risk. So there are people who are low risk with LP little A, people who are intermediate risk for LP little A, and people who are high risk for LP little A. This is gonna be difficult if you're just on the border, right? If you were borderline between moderate and high risk, yeah, you're gonna probably change risk categories depending on how you test or when you test. Um, but for most people, you are gonna stay in the same risk bucket, even if your level fluctuates by 10 to 20 percent. Uh, and really trying to figure out again, all the lipoproteins, this is risk that accumulates over decades. So, what is your general average? Is your average in the intermediate or high risk categories? Then you should think about how you're gonna try to mitigate that risk. Um, the current recommendations is that we test LPA once for everybody, and that is enough. I do think a couple of tests, especially if you're on the borderline, might be helpful. The other thing is for women who are moderate or intermediate risk, getting tested post-menopause may also be informative because women do tend to have an increase in LP little A post-menopause, uh, especially if they are not on estrogen replacement therapy or uh other menopausal hormone therapy. So that might also change your risk calculations a little bit for yourself. If you're not gonna change your management based on the different data point, then don't do it. Um, but I don't think that trying to test every year is particularly worthwhile. Whatever risk bucket you're in, make your decisions about how you're gonna do deal with your residual risk appropriately. And probably, you know, two tests in a lifetime is is more than adequate for most people. All right. Andy Billy, good to take vitamin K with D3. If K is good, what dosage is suggested? Vitamin K. Um here is another great example of things I do that are not as evidence-based as I would like for them to be, because the randomized controlled studies on vitamin K, particularly K2, uh, which is the like MK7, MK4, and the uh vitamin K that tends to be found more in animal products than in uh leafy green vegetables, which is also K1. The K2 seems like it should be a really good idea. It works on something called matrix GLAA protein and helps reduce or helps tell the body where to put calcium, right? You eat dairy products, you have uh replete vitamin D levels, which means you're absorbing the calcium, then it gets into your body. Where does it go? You would love for it to go to your bones and your teeth. You would not love for it to go to your heart valve or to your blood vessels, but you need a signaling molecule in your body to tell the calcium where it's supposed to go, who's gonna use it. And the matrix GLA is what helps signal that. And so, for all of these reasons, there are a lot of good ideas about using vitamin K to like help move calcium into the bones and teeth and not deposit it in your heart valve or in your artery walls. Uh and at the epidemiologic level, we all know how that how we feel about those studies, especially nutritionally. People who eat more vitamin K rich foods and who have higher levels of vitamin K do seem to have lower rates of cardiovascular disease. And we thought, amazing, this is a miracle. We're all gonna take vitamin K. We're gonna take all the calcium out of our heart valves and put it into our bones. It's gonna be a miracle. And it never works, right? It has never worked out that way. In a randomized controlled clinical trial, when we've studied vitamin K2 administration, we have not been able to show that even for calcified aortic stenosis, like the valve problems, vitamin K has not yet been shown to reduce the progression of that disease. It has not been shown to reduce progression of arterial plaque. However, it is very safe. We have never shown a problem with the administration of vitamin K. Uh for the, and this, by the way, is the caveat to this is for people who are not on vitamin K agonists or antagonists. So if you are on warfarin or cumidin uh to thin your blood, this is different for you, right? You should probably not be talking, taking vitamin K or eating vitamin K rich foods without talking to your team about that, because it will change your INR levels. Um, I'm hoping that most people are getting away from warfarin and cumidin unless you have a mechanical valve because it contributes to calcification in the arteries, probably related to the vitamin K antagonism. And uh that is that is a whole separate conversation if you're on blood thinners. But for the rest of us, if you are interested in vitamin K rich foods, that's great. And there doesn't seem to be any harm associated with increasing your intake of vitamin K. So even though there is no randomized controlled trial that supports the use of vitamin K, I take my D3 with vitamin K. That said, because there's no randomized controlled clinical trial that tells us that it's doing anything, do I have any idea what dose we should be using? I do not. I'm not sure anybody knows what dose we should be using. Some studies say that MK7 is better. Some studies show that MK4 is better. I honestly don't really feel strongly about this because it's kind of a like probably it's a nice idea. Maybe it's helpful. If it's helpful, it's probably helpful in the long run. I do think increasing your intake of vitamin K rich foods is probably a good thing because that's going to drive you to a more whole food-based approach anyway. That's a good idea. But, you know, I don't I pay much more attention to vitamin D dosing, which I dose, by the way, based on people's lab results. Uh, I do not spend a huge amount of time worrying about the vitamin K dose or how much MK7 is in their supplements. Okay, neat. Let's hold plastics companies accountable for environmental damage. Uh sure, sounds good. Let's do it. How important is being in ketosis when trying to stabilize plaque? I have a CAC, a CTA, and a CIMT. So for my patients who are on a therapeutic carbohydrate reduction approach to nutrition, um I don't think driving ketones is that important for stabilization or reduction of plaque. And some of you are going to come at me about nobody should be on a ketogenic diet for heart health. Therapeutic ketosis is a biomarker. It is not actually a way of eating. And so there are vegetarians who achieve therapeutic ketosis. There are some vegans who achieve therapeutic ketosis. And uh the reasons in my mind that I have seen to chase ketones are for brain-specific indications, epilepsy, severe mental illness, uh, or cancer seems to be another physiologic state where driving ketones up may be interesting. The last part I would say is that there are maybe some interesting ideas about ketones as fuel for the cardiac myocytes, the heart muscle cells, which by the way seem to prefer fatty acids and ketones as a fuel source rather than carbohydrates. If you have heart failure, I am curious, but I have no data. I am curious about the possibility of ketones as a way to potentially alleviate some stress on the heart cells. That is total supposition and curiosity. Again, not a lot of evidence for that, although some people have used it and studied it. I'm not sure the data support me recommending it for my patients who have heart failure yet. But I think that's probably the next frontier. But that's different than plaque stabilization or plaque reduction. In general, if people are coming to me just for plaque stabilization and reduction, a ketogenic diet is not necessarily the approach that I would take. There are a lot of reasons that I, again, from my much broader health standpoint, do not argue with a ketogenic diet or even a carb restricted diet for insulin resistance. But this is this is a, again, a conversation about people's personal goals. I've had patients that got, anyway, um, nutrition is complicated. And my recommendations are very, very different based on what people's goals are and what their chief complaint or where they come to me is. I do sometimes recommend carbohydrate reduction. I sometimes recommend a like very plant forward Mediterranean approach for other patients who want that as their as their strategy for managing their cardiovascular risk. All of that has evidence to support it. So, all that to say, I don't think ketosis is important for plaque stabilization. In Denmark, doctors don't do TRT. What is my opinion? Uh again, TRT is not, you know, I am much more comfortable doing women's menopausal hormone therapy than I am doing TRT. I do TRT for many patients, but it's um I'm not as much of an expert on that as I would say I focus on the female side of things. All of this hormone replacement, I got into because I thought it was important for whole person health and for helping people manage cardiometabolic risk. So again, we talked earlier about the role of testosterone in cardiometabolic status. Um, I think there is potentially some signal there for improving insulin sensitivity, particularly in people who are training well and doing a lot of exercise and movement in their in their daily lives. Um but I am not certain that by itself, in the absence of any other lifestyle changes, it's enough to really move the needle dramatically. And depending on how you're doing it and what the dosage is, um, there may actually be some risk to it. I think that that's overblown in a lot of the old studies. But um, you know, why an entire country doesn't do HRT, I don't know. Um Are those of us who suffer with inflammatory bowel disease along with psoriasis or eczema with IL-23 at greater risk of coronary artery disease? Great question. I think that pro-inflammatory states are absolutely associated with general increased risk for cardiovascular disease, but those particular afflictions are not ones that typically track. So it's much more common for uh lupus and the like anaphospholipid syndrome, uh rheumatoid arthritis, and all those things. I'm not exactly sure what the hazard ratio is for inflammatory bowel disease and psoriasis or eczema. Um, it's probably some, but I don't think that it's as great as, for example, the the other autoimmune conditions that I mentioned. But I don't actually know off the top of my head. We can look that up. Uh, would doing martial arts be good for heart health? Exercise in general is great for heart health. And I break exercise down for people into four different buckets. Again, not my not my own creation, but uh cardiorespiratory fitness is important. That comes with base training and interval training. Resistance training is hugely important. Um, I personally lean into that pretty hard because I think it's the most fun, and uh I think it is great for overall longevity. I think muscle is a very important endocrine organ, right? It's our biggest utilizer of glucose in the body, and certainly the one we can influence the most in terms of, you know, the liver uses a lot, but we can't necessarily impact that day-to-day. We can impact how much our muscles are using glucose. And then the last one is things that are mobility and coordination related. So that includes um dance, yoga, Pilates, martial arts. And so some of those things count for multiple buckets, which is very efficient. And I think that's amazing. Um, martial arts is a group sport, right? It's a group in event, and that brings with it some social connection and some interactions. It is highly dependent on uh like mind-body connection and coordination. So those are all amazing things above and beyond the heart health specifically. So uh if that is your jam, please continue by all means. I think it's probably good for your heart, good for your brain, and good for your overall longevity. Do you think that CIMT will be added as a screening test at some point for CVD nut that automated edge detection has greatly reduced technician variability? So uh, Paul, I think probably not. Um, as much as I love CIMT and as much as I still advocate for it and use it in my practice, uh I am concerned that they're, you know, the the heart doctors are very heart-centric. CIMT is, of course, a carotid artery test. It can also be a femoral artery test, but it's not the heart. And the heart doctors love taking pictures of the heart, and they want to know about the coronary circulation above and beyond everything else. The information we get from plaque detection and IMT in the carotids and the femorals is highly correlated with the amount of disease in the coronaries, but it does not necessarily drive you to get more procedures done in your coronary circulation like stents or cardiac angiograms. And uh it is still an indirect measure. So even though it is no radiation, even though we repeat it annually and we can follow people's progression or regression of disease or stabilization of disease, um, currently it is actively not recommended by the American College of Cardiology. It would take a like moving heaven and earth to uh make that into a class one recommendation where they actually recommend doing it instead of not doing it. And uh I think CT Angio is probably gonna be what takes over for many people as the as the screening and and detection tool of choice. I hope that CIMT will and plaque detection. So IMT is one thing, that's the thickness, but also using a protocol where we detect plaque, um, which is not something yet that AI has totally figured out how to do. Uh, there is a preventive cardiologist who has done a lot of very interesting publications in sort of automated protocols and using an immediate feedback system to allow you to, you know, have basically have a minimally trained technician do a complete scan and focus on certain areas so that you're getting real-time feedback as the scan is progressing about, oh, hey, you know, image this area again, take a different angle, change this setting, and see if we can like the the machine thinks it sees a plaque, and even if the technician doesn't, the machine may be able to help us find that, quantitate that, and create a total plaque score that is going to be much more reliable than the than the current um technician-driven protocols. The cardio risk protocol is very specifically designed to help minimize the variability, but that's the scanning protocol. That is not the automated edge detection that's really making IMT more reliable. The issue with edge detection versus the scanning protocol is if you only have one picture for automated edge detection, that is one piece of a three-dimensional structure. The reason the cardio risk scanning protocol is so effective at minimizing variability is that we are taking deliberately three separate images of the entire back wall of the carotid artery and doing that in a way that allows the lab to make hundreds of measurements across each of those images. Then we have both sides, right, right and left side. And all of that combined gives us a very, very precise estimate of the internal medial thickness down to hundredths of a millimeter. And I think that is, you know, above and beyond the automated edge detection, really what is going to help reduce the variability for IMD. But the ability to detect plaque still depends on the eyeballs of the person doing the ultrasound in that moment. And the ability of that sonographer or technician or physician, depending on who's scanning, to see it and then take a good picture of it. And that so far has not yet been automated. And until we get that part really down, uh, we're not gonna be able to use CIMT with plaque detection as as effectively as we can use a CT scan. All right, David, what are your thoughts on Greek yogurt with 0% fat? Um, Greek yogurt is one of several foods that seems to be very beneficial for the microbiome. And dairy in general seems to be a slightly separate, especially fermented dairy or dairy with uh active cultures in it, maybe a slightly separate category of risk than regular foods with higher fat content, especially high saturated fat content. Recent paper came out showing that full-fat dairy seems to have a differential impact on cardiovascular risk factors than you know, other high-fat foods. So I tell people Greek yogurt is a good food to eat if you're gonna include dairy in your diet. I don't feel strongly that it needs to be 0% fat. I don't feel strongly that it has to be whole fat. Uh, Greek yogurt is generally unsweetened. So, again, my concern with a lot of the more processed low-fat dairy stuff is that it tends to be higher in sugar as they remove the fat content. For Greek yogurt, it's not gonna be that much higher, or it's probably not at all higher in sugar if it's 0% fat, but um sure, sounds great. I prefer the full fat version for myself, but uh I think the zero fat is fine. All right, I'm gonna go back to our anonymous questions here for a second. There are some drawbacks for people with PAD or CAD in taking vaccines, like the COVID shots. Have I heard of PAD or coronary patients having issues after getting a shrink's vaccine to prevent shingles? Are there any tests a patient can ask for prior to getting the vaccine to ensure there won't be adverse reactions? Uh I am unaware of any testing that can be done ahead of time to look for risk for adverse vaccine events. Uh, I have personally not seen a patient who's had an adverse reaction to the shingles vaccine. I know that they can be very immune-provoking, right? People get a lot of uh injection site reaction or a lot of myalgia. Uh, some people get fevers and chills right after their vaccine because, again, the intention of a vaccine is to stimulate the immune response. I would not be surprised to hear that somebody's had an event after a vaccine, meaning a plaque event, heart attack, stroke, or limb event. Um, but overall, I think our evidence supports, I mean, that there have been some very interesting papers looking at the use of the shingles vaccine and reduced risk of dementia, is one of the very few things for which uh we've actually seen an improvement over time in rates of dementia. So vaccines are a touchy topic. There's a lot of difference between types of vaccines. That is not a conversation I am prepared to engage in today for uh probably obvious reasons. And I don't know of any testing that can be done ahead of time to know whether you are at risk for a for vaccine harm. So sorry about that. Um, but I I do think that vaccines are not the same as they used to be, and they are not all um not all bad. All right. Best test for soft plaque, Stan Man. Uh best test for soft plaque is either a CT angiogram or a CIA or carotid ultrasound test. If you are younger, you may also want to have them image ephemerals. Um, but soft plaque right now we can only detect on a CT angiogram or a an ultrasound test. So which test is best for you really depends on what is available near you and what your budget is. So there are people who live in a place where that's really not easy to get a CIMT test done. C CTA, carotid angiogram, I'm sorry, coronary angiography, uh, and a CT scanner is pretty much available everywhere, but the price is much higher, and getting a doc to order it for you is not always straightforward. So the best test is whatever one you can actually get done, but it should either be an ultrasound-based modality or a contrast with dye-based modality as opposed to a calcium score, which is non-DIE and will only image that hard plaque. All right. Do I know any institution other than Clearly that does CT angiography with AI? Yes. So uh Heartflow is the other company that is big in the space right now. They have the FFR CT, which will do the uh flow reserve test to look at the degree of narrowing and whether that's causing significant drop in pressure across the narrowing. They also have a plaque analysis tool uh that is on par with Clearly. Both of these are a little unknown, in my opinion, with respect to their reproducibility and reliability. And some of this come came out of the of the you know Feldman's work. Some of this is just listening to people who have sent scans to both Clearly and HeartFlow, same patient, same scan, and gotten different answers back. So we just don't really, it's newer technology, it's very exciting. Everybody likes the pretty pictures and the nice, highly quantitative reports. What I don't know is if you have a CCTA and your plaque analysis, whether it's HeartFlow or clearly, comes back and says, you know, you have 400 cubic millimeters of uh, you know, soft plaque, and next year it's 450. How reliable is that change? Is that real change that we believe is a true increase by by you know over 10%? Or do we think that that's within the margin of error of that test? Or is that within the algorithmic drift of the ability of the tool to detect change? I don't have great answers from these institutions yet or from the research community yet about just how reproducible and precise uh these tests are in these algorithms. Some of the literature using CCTA has been done at, you know, independent labs. It's not using clearly or heart flow. Others have used clearly in heart flow. Right now, I think the technology is so new that it's very interesting and it certainly helps us get a baseline and know how much very soft, vulnerable plaque there is. But using it to follow disease over time, I'm just not quite sure I understand exactly how much change is real change. So that is the big unanswered question in my mind about these technologies. We are gonna get there. Uh, they are gonna evolve with us, but for right now, it's still a little bit new and um perhaps not as not as unreliable. I'm sorry, not as reliable. Uh all right. Okay. What would be your speculation hypothesis about a man with less than 60 APOB but greater than 200 LP little A? And as how taking super physiological androgens may impact ASCVD, uh, considering how anabolic steroids raise APOB but lower LP little A. Um. I just don't know what the you know, there are so many issues with the with the performance enhancing group of substances, um, including off-target effects, including uh meaning like whatever they're doing to the lipids, what else are they doing to the liver? What else are they doing to inflammatory markers? What are they doing to um our hemoglobin and hematocrit? Are we, you know, is the body working harder to to pump blood? All of these things are unknowns to me. I just don't have a sense for any of that. Um and I don't know what is due to androgens themselves, what is due to the off-target effects, and what is um yeah, unclear. Totally unclear. Sorry. All right. Do I worry about the use of beta blockers? Uh I don't know exactly how to interpret that question. Beta blockers have lots of different applications. They are one of several drugs for blood pressure control. Some people use them as part of gold-directed medical therapy for heart failure. Uh, there's a lot of information about taking them after heart attack that has evolved over time. My impression is that some patients tolerate beta blockers really well. Some people use them for tremors, some people use them as you know, intermittent drugs for uh like performance anxiety. Some people find that they are miserable on beta blockers and have a lot of symptoms with them. And if that's the case, then I think there are a lot of other drugs that we can use to deal with whatever the indication was. Um, but I don't know what what specific worry you might be referencing. Can people live a long life with stable angina? Yes, absolutely. Uh, it does imply that you have plaque that's caused narrowing. So let's figure out why you have plaque and see about reducing your residual risk. The angina itself is probably not the issue. The issue is what other areas of unstable plaque might you have that could rupture and cause an event. So just like people live long lives with cloudication, most people never progress to limb-threatening ischemia or problems with you know being at risk for losing the leg, yes, you can have stable angina, but what was the disease process that got you to stable angina? Is that disease progressing? And how are we managing your residual risk? If all you have is the stable angina and everything else is looking perfect by itself, that should be fine. What we worry about is what the underlying disease process is and how are we gonna get there? Okay. For high cholesterol, as far as slow-moving cholesterols, my functional doctor suggests repatha may be better than statins. So better in what way? It reduces LDLC uh significantly above and beyond what statins do. It reduces LP little A, which statins do not, and the side effect profile does tend to be better. I, if I can, like using Rappatha in many of my patients, um, getting access to Rappatha is a little more challenging. So it is much more expensive, and most insurance companies are not paying for it until you have quote unquote failed statin therapy. That is, again, something that you and your team will negotiate. Um, I think that PCSK9s are great drugs, but you know, they're drugs. And um, but in terms of the things people worry about with statins, people worry about the muscle interaction, not only just the myalgia and the pain, but also is it actually toxic to the muscle? Is it damaging our muscles? Um, our muscles, again, are a metabolic organ, they're using, they're disposing of glucose. Is this the mechanism by which statins are causing insulin resistance in some people? Very possibly. Um, I find that at low doses, patients tolerate satins pretty well, and I don't see a huge impact on insulin resistance unless I have a very brittle type 2 diabetic or even a type 1 diabetic. Then I actually do sometimes see changes in their sugars with this, but um the repatha seems to do that substantially less. It does not have muscle as a target organ, so that's great. And uh again, we do get some benefit in reduction of LP little A. And those, for all those reasons, I do like PCS-K9 inhibitors. Uh, access to them is still kind of a problem. But if you know, cost were no object, um, personally, would I prefer a PCS-K9 to a statin? I probably would. How helpful is ENOS enhancement from dietary nitrates and L-citrulline for improving early CVD? Um, Paul, that's an amazing question. I have no idea how impactful it is. I think I like monitoring ADMA as a metric for nitric oxide activity in our vessels. Again, it's one of these things that I do because it makes a lot of sense to me. And I think the downside potential risks are quite low, but I don't have a huge body of evidence that supports that we will do this and like make these miraculous changes. I do it because it makes sense to me, not because there's a great evidence base for doing it. Some people seem to respond well to like. Dietary nitrates. Some people do well with citrulline. Some people actually also need arginine with the citrulline to get a good impact. You can check ADMA, you can check flow mediated dilation, although that as a metric is not something I really like in my practice, and I'm not sure that the evidence base for it is all that strong. I think exercise is probably the best driver for improving nitric oxide synthesis. There are some interesting other tools that are out and about. I was learning about enhanced external counterpulsation therapy recently. This is something that is used in patients with stable angina. At least that's its approved indication. But I had another patient who was taking it for or using it for other reasons. So essentially these huge blood pressure cuffs that go all up and down the leg and they fire in timing with your heart rate so that you're changing the amount of strain and increasing shear stress in the artery wall. And increasing shear stress improves nitric oxide. And these ECP therapies have been shown to actually reduce high sensitivity C reactive protein, improve nitric oxide metrics, including flow-mediated dilation. So there's a lot of very interesting tools and technologies available. There are supplements that are available. How much they move the needle, I don't know. Do they move the needle above and beyond a lot of like high-dose exercise and people who are very active? I don't know. Is it gonna hurt you? Probably not. So let me know how you feel about it and what you've noticed in your own life. Okay. Guys, these are amazing questions. You are showing up in a big way. I am so excited. Thank you guys for all this. This is so much fun for me. Okay, I hope you guys are having a good time. And um, based on the amount of engagement we're getting, we are absolutely going to do this again in the future. Thank you. All right. NNRQ 822, what is the best way to lower your heart rate and prep for a CT scan, like heart felt or heart flow or clearly? So your CT scan protocol, the um team there will actually probably give you a beta blocker, uh, depending on what your resting heart rate is, to try to get it low enough. There are some people who have to come back or who are actually not that responsive to beta blockers and have a hard time getting these CT scans done. Uh, if you want to use biofeedback, then I would say the best way to is to see if you can actually modulate your own heart rate using things like breath work or meditation practices. And uh, you may find that that's pretty effective for you, but you can practice doing that at home, which has the ancillary benefit of helping improve your vagal tone, improving your parasympathetic nervous system response, and reducing your physiologic and perhaps also your mental stress. So great tools. On the subject of stress test. Stress test seems like a waste of time ordered by your cardiologist, JP. Yeah. Um, your goal is level five, three pests, three friends who passed the stress test and had mild MIs within five months. Yeah. I again in my prevention space, like the people that I talk to, we are we are less and less enamored with the stress tests, but I think the mainstream cardiology community is still really in favor of them. You know, we are not great at predicting who's gonna have a heart attack. Like we know who's gonna have plaque pretty well, right? Framingham risk was the 40 years ago approach, and we've come a long way since then. We can detect, I mean, we can predict pretty well who's gonna get plaque, but who's gonna destabilize and rupture a plaque and actually have an event? Our ability to predict that, and especially the timing of that, it's not amazing and not very reassuring. Um uh relax, sleep, become. I saw your video showing HIT training helps reduce atherosclerosis. Do I have any HIT programs available to follow? No, not personally. The protocol in that study was the very well-known Norwegian 4x4. So this is um a protocol where you're gonna do four minutes at high intensity, and that intensity is defined by your max heart rate, which is again determined by your age. Um, that's a pretty simple calculation. It's all available in that video or at least in the study protocol. DM me if I didn't actually do it in the video. Um, but the Norwegian 4x4 is four minutes of that high intensity with three minutes of moderate recovery repeated four times. I have started doing that uh as part of one of my workouts during the week, and it is um definitely challenging. Make sure that you do a good warm-up first. You should be warming up for at least 10 minutes, probably at low to moderate intensity based on heart rate, then doing your four by fours, which again is actually four minutes of the intense, but three minutes of moderate recovery four times, and then do a nice cool down. Don't forget your stretching, guys. I forget my stretching and I feel it. It's not great. Don't be like me. All right. Hi, Dr. Johnston. What's in a plant? Is there a way to test the type of particles that make up LDL? Small particles, large buoyant, yes. So you can do particle analysis. The most uh there's two ways, ion mobility and NMR are the two that are currently commercially available. I personally prefer the NMR, but I think both are valid, and just make sure that you, whichever one you use, keep using that one if you're following it over time. The more important question is how important is measuring the particle size and particle number and all of these like advanced lipid metrics. There is a lot of correlation between the size of your LDL particle and the metabolic health, right? So patients who have low triglycerides, high HDL tend to have larger sized LDL particles. These are a little less likely to be oxidized, but the myth that the large buoyant particles do not get retained in the endothelium or in the vascular wall is not really correct. It is less likely, but it is not impossible. It is not like these are big beach balls that bounce off the side of the artery wall, whereas the small ones all get in there. Um, the lipidology community has largely moved away from the fancy lipid testing and the NMRs. I still like it mostly because patients like it, but I don't love getting trapped in this, you know, my particle count is 3,000, which is quite high, but they're all big, so they're probably not an issue. I much prefer to have the conversation about imaging. Like, do you have plaque or not? If you have plaque, it doesn't really matter to me that you are part pattern A and that you have large buoyant particles. You have particles that are oxidizing in your artery walls as we speak, because I can see them on your CIMT or on your uh carotid ultrasound, and we kind of have to put the fire out. You know, if you have a particle number of 3,000 stochastically, right, just by the sheer volume of particles circulating, uh, this is probably contributing to ongoing plaque formation. Now, if you have a particle count of 3,000 and you're 70 and you have no plaque anywhere in your arterial system, well, then does it matter if they're large and buoyant or or not? Like it doesn't matter what the size is. If you don't have plaque, we can talk about whether it still makes sense to manage that number or not, but I'm a lot less concerned about that if there's no evidence that they're being retained in your endothelial space. So while I still order NMR testing, I do find it interesting in a lot of ways to talk about that as a metabolic health marker. I'm not sure that we make a lot of therapeutic decisions about whether we treat your APOB numbers based on that. I much prefer to make that decision based on your imaging, whether you have plaque or not, your symptoms, and your own philosophy about how you want to manage your residual risk. All right. Hey Andy, thanks for the wave. Glad to have you here. All right. Peter, why would you want to reduce calcium uptake in your arteries? It protects by converting soft plaque to heart plaque. Yeah, so um again, mostly this is about plaque at all, right? It's not so much the calcium drives plaque formation. And uh some people would just as soon see if we can regress the plaque or have, you know, reverse cholesterol transport take away some of those soft uh lipid-rich plaques before they actually end up calcified and potentially causing some narrowing of the artery. But I think especially reducing it in the arteries is good for the valve, your aortic valve in particular, right? If that gets a lot of calcium buildup, it does not open and close as well. And that can be a problem. It's why people sometimes need their aortic valve replaced. The other issue, um, in particular for a lot of my patients with long-standing diabetes or kidney disease, is that the calcium doesn't necessarily stabilize plaque in the artery walls, but it just accumulates there and it makes them very stiff. And stiff arteries cannot dilate no matter how much nitric oxide is around, right? They just become this lead pipe. And if the arteries are not soft and expansive, then the there's a lot more stress on the heart, there's a lot more stress on the vascular system, and then we actually are more predisposed to forming plaque. So the deposition of calcium is not only about stabilizing plaque, it is also about the general stiffness of the artery wall. And we would just not want that. We would much rather have them be soft and compliant. K2 may assist in reminiscing our teeth. Yes, exactly. Um comments on Rapatha, Owen. I think I answered that one. I hope you got some satisfaction of that. Um, all right. Lipoprotein A, 216, Lipo B 153, cholesterol 325, triglycerides 85, 007 Tinkens, is my forest on fire? Um, great question. It depends a little on your CAC is zero, so that's great. Um, but we don't know about any soft plaque and we don't know about your family history. I don't know about your inflammatory markers, uh, all of that contributes to whether the forest is on fire or not. So, you know, when I see patients like you in my practice, the next step for me is to get my ultrasound out and take a look at the arteries and see what I see. Uh, if that's not an option or if I'm seeing you remotely, then we would think about other ways to get imaging to see what's going on. CAC of zero, depending on your age, is really different, right? If you're 40 and your CAC is zero, I have no idea. If you're 80 and your CAC is zero, I feel much more confident that your forest is probably not on fire at this point because uh that is well below 50th percentile for age. So that would be, you know, a really good uh outcome, but we just don't know without knowing your age. All right. Sam saw my cardiologist yesterday, got some labs done. Strong family history of heart disease. When I raised family history, he added Zedia to my lipid dose of 40 milligrams. Question, question. So um the new guidelines are talking about the thresholds. How low is low enough? This is gonna trigger some people. Um, but strong family history would be an risk-enhancing factor. And that therefore, you would probably want a lower target for your APOB or LDLC, again, above and beyond your overall metabolic health, right? And we can argue about whether that target should apply to people who are in optimal metabolic health. And if so, you know, why do we have evidence? No, our evidence is in a general population. Our general population is overall, unfortunately, not very metabolically well. So I don't know whether these thresholds should apply to you, but adding Zedia to your statin is a way to try to drop your LDLC even lower because that physician believes that your family history is a risk-enhancing factor that probably moves you from a goal of less than 90 to maybe less than 70 or less than 100 to less than 70. Uh, you could also say, well, if I get there, should I drop my statin dose a little bit? Maybe, right? I personally would prefer people on low doses of two medicines than a higher dose of a single medicine. That is a personal preference, not necessarily evidence-based or data-driven. Um, but I find that people tolerate that better and we get fewer side effects when we do that. Downside is more stuff, more pills. All right. Paul Elkins, for women who used HRT for five years post-menopause and then stopped per the old guidelines, does their tenure window start only when they were not exposed to estrogen, premenopause, or HRT? So the window, when does the window start? The window probably starts when they stopped their replacement therapy, but let's talk about what the window means. The window for hormone replacement therapy talks about when do we see cardiovascular benefit and maybe after which point starting could be harmful. But I think that the window for harm really depends on what hormones you're using. Conjugated equine estrogen and madroxy progesterone acetate, what was used in the Women's Health Initiative, is not the same as what most people are using today in modern postmenopausal hormone therapy, which is estradiol and micronized progesterone. Conjugated equine estrogen is uh activates something called MMP9, matrix metalloprotenase 9, which is something that will eat away the fibrous cap over a plaque, causes plaque destabilization and plaque rupture events. So women who were in the Women's Health Initiative who started late had increases in MMP9 and plaque rupture events in the first year of starting HRT. We do not see that with estradiol. There is no evidence that estradiol increases MMP9 or destabilizes plaque. I do not think that there is an unsafe time to start menopausal hormone therapy for women if they are having symptoms, meaning genital urinary syndrome of menopause, uh hot flashes, night sweats, whatever the case may be, if you are having symptoms in menopause, we should manage your symptoms. That does not mean you're gonna get cardiovascular protection, but I don't believe that it is harmful. And that is an important distinction. Now, if you're talking about when do you get cardiovascular benefit, that probably has to do with downregulation of the estrogen receptors that will start when estrogen goes away and stays away for a period of years. So from that standpoint, um, you know, you probably the woman you're referring to got an extra five years of protection with estrogen receptors that were probably still happening and and happy in the endothelium, uh, and would start downregulating only when estrogen really went away. So that clock would start at the time of you know postmenopausal estrogen or estradiol levels. I hope that is at least a little helpful for your question. All right. Sam, more information about your family history. Yeah, thank you. Um JP, if one has a clear CT angiogram, is there really any point in getting a stress test? Uh I don't think so. What are you gonna find? Um the only possible exception to this would be women with small vessel disease. So um, minoka inoka, there is a category of particularly women who have anginal symptoms, meaning chest pain, uh symptoms with exercise, who actually do not have severe plaque in bigger heart vessels on a CT angiogram or on a regular uh invasive coronary angiogram, but they have small vessel disease. Um stress testing is one way potentially to uncover that diagnosis. Um, special kinds of angiography in the cath lab uh with medications that will cause the heart to react in a certain way. I'm not an expert in this, but they can also uncover that diagnosis. Um, but it's a pretty specialized case where people are having symptoms. If you're having no symptoms and there is no evidence of blockage on your CT angiogram, I don't think a stress test really adds any additional value because it's unlikely to be positive. If it were positive, they'd look at your CT angio and say, there's no blockage here, we don't know what's going on. Um, but it's an interesting question. I would have to actually run that by another cardiology friend just to see what they would say, but I don't, I can't think of a good reason to do that. All right, William. Since we now emphasize the time of exposure of the endothelium, why not start taking medications while you wait for lifestyle and diet modifications to take effect? This is a personal philosophy question. Um all of these are great points, and I think a lot of people are wanting to try to do this with lifestyle alone, which is a reasonable approach. There are a lot of people who have a strong family history who are deathly afraid of a heart attack, and starting medications early is also a reasonable approach. There are side effects to medications, there are possible adverse consequences to being on medications. There is the medicalization of all of this. And people in the medical community talk about this. Like, are we making everybody feel like a basket case and giving them a diagnosis when in fact they're okay? I don't have answers to this. This is again where I sort of say, I work for you. You tell me, as you if you're my patient, what makes the most sense to you, and I would like to enable that for you. Some people do not want to be on medications at all costs. Okay, that is their philosophy. Um, from a like population health standpoint, just stepping back and thinking about it. If you have an optimal lifestyle, should you keep your LDLC as low as possible? Maybe, but how many people do we have to have an optimal metabolic health and drive LDLC lower to change the event rate? I don't know. We don't have the answer to that because again, our overall population is metabolically unwell. And so this is all confounded by that baseline population. And I understand the argument that says LDLC is or ABOB, however you want to talk about it, LDL particles are causal, but they are not the most important risk factor. So this all depends on, you know, how does taking medication impact how you see the rest of your risk? Um, I, you know, if you're doing all the lifestyle stuff anyway, sure, go ahead. Um, include the medications. If you think that taking, you know, five or suvastatin is going to immunize you against heart disease, and therefore you don't have to pay attention to your nutrition or exercise, then I would say that is counterproductive. And again, every person's brain works a little bit differently, and how they view all of this just it adds up for some people and it doesn't for others. And I think all of them can be very reasonable approaches. This is so unsatisfying if you are looking for one answer. And I'm sorry about that, but also not sorry because I think that that's how I practice medicine and um what I think is right for everybody. Comment on CAC and endurance athletes. I ran four times a week at 440 Km for 15 to 18 KM. Is La Plaque correlated with CVD or any risk if you compare athletes with versus without it? So the again, when you go back and look at that video I did with Dr. Brad Stanfield, sorry, Kiwi, not from the UK, my bad. Uh, we talk about this idea, like what defines an endurance athlete. The training volume is quite high to be considered an endurance athlete. And again, those are people who were uh also very young when they started training, most of them in their 20s. Some of the the older athletes were actually starting endurance training in their 30s. Uh the general sense is if you take a very well-trained fit person with a CAC of 300 and you compare them to the average person in the population with a CAC of 300, the very fit athlete is going to have less but not zero risk associated with that CAC versus the average population control person with the equivalent CAC. So there's a lot of protection that is gained from your fitness, from the exercise and the metabolic flexibility, but it is not an immunization, right? The CAC of 300 still means you have risk. You still have plaque there that could potentially be destabilized depending on how old it is. Um, but your risk is a lot less than the average unwell, not fit person with a CAC of 300. Marcy, question Do we need to get both C I M T and a C A C or can we just start with a C I M T and then if shows plaque, do a C A C to show more? Uh again, I think it depends on how much you want to know about the heart, how much you want to know about soft versus hard plaque, how is it gonna change your management? If you are not having any symptoms. And you don't have a strong family history, and your CIMT shows a small amount of soft plaque, you could do a CAC, but I don't know how much it's going to change the management. If you're really worried about your coronary circulation after your CIMT results, I would almost argue that a CCTA or a CT angiogram might be more informative because then at least we can potentially get the CTFFR and know: is there a narrowing here that's really significant? Right? Not just like, is there plaque somewhere? Um, but how much is there, how much narrowing is there, where is it, and what evidence do we have that going after it might improve anything? If you're having symptoms, for sure a CCTA is the way to go. Uh this all all of this like sequential testing really depends on what is available to you and how is it gonna change what we do next. All right. Rick, I have 40% blockage. Should I watch total fat or only saturated fat in my diet, age 73 on statins, low dose aspirin, and lysiniprome? The best evidence for the relationship between dietary fat intake and LDL cholesterol or APOB is for saturated fat. There are people in the prevention space, like Dr. Esselstein, who would say that low total fat is important. There is also evidence that to manage insulin resistance, you can either go very low carb or very low fat. So what we're figuring out for any individual person is what's the thing we're trying to fix? Is it insulin resistance? Is it apOB? Is it both? What is appropriate and sustainable? Everybody should be working on trying to get as much whole food as possible, right? Um, as little packaged and processed, I know processed is a loaded term, but again, it's like a lot of other things, you sort of know it when you see it. Um direction you want to go with your nutrition depends a lot on what makes sense for you, what makes sense for your family life, what makes sense for your day-to-day sustainability. Uh, if you're trying just to manage LDLC and Apo B, evidence would suggest that reducing saturated fats helps with that. The community in the low carb space says that saturated fat has been demonized. I think many of those studies were potentially confounded by trans fats. Um, but the evidence for fat intake is a little mixed. Fat is an energy source, so are carbohydrates, but you have to have one or the other. And I do think that having some metabolic flexibility and being able to run on one or the other is potentially very useful. Uh, but the swamp is the middle ground, right? Swamp is where we have sort of a lot of bad carbohydrates and a lot of bad fats, and our metabolism gums up and nothing works very well. So this is this is not a straightforward question. The evidence is a little bit mixed, but um, if you want the answer that will drive your LDLC the lowest, the answer is low saturated fat. Total fat is less relevant, but you'll find that it's hard to reduce your saturated fats alone without reducing total fat. You'll some of that will come down. Uh, but if the answer is, you know, do I reduce all animal products from my diet because I believe in Dean Ornish and Dr. Eselstein, then you're gonna end up with a very low fat diet completely. And I personally think that that has, yes, there's evidence for it. I'm not sure that it is the most appropriate strategy for all people. Um, if it's working for you, I'm not gonna take it away from you. Okay. But if you don't want to do that, I think that there are slightly more moderate approaches that emphasize um whole food-based fats from olive oil, avocados, uh, right, whole food sources, uh like a Mediterranean-based approach that can be very reasonable and appropriate. William, children in the most active growth periods have APOBs in the 30s. I am shooting for the 30s, I am in secondary prevention. Yeah, the um the argument that our population levels of APOB have actually considerably increased over time and that our standards are much higher than they ought to be has been floated. I am not uh as familiar with this. What I'll say is that you know, cholesterol in general is a very interesting molecule, and what circulates in plasma versus what is available in each individual tissue in the body is always interesting. Um, certainly the interventional studies have not shown a risk of harm for dropping APOB very low thus far. That is my interpretation of the literature thus far. David, taking 81 milligram aspirin makes sense for 76-year-old male, type 2 diabetes, 850 CAC, and maybe elevated lipoprotein little A, depends on what the uh what the units are for that. If it's metal grams per deciliter, 85 is elevated. And um, so we are having an aspirin video come out very soon. The answer to this question will be in that video. I would love for you to subscribe so that you get that. And I will say both elevated CAC above 300, uh, even above 100, and elevated lipoprotein little A are gray zone indications for aspirin use. Uh, if you've not had an event, you do not automatically meet criteria for using aspirin. However, I would say um there are a lot of patients in my practice who would be on an aspirin for those types of indications, recognizing that aspirin is not risk-free. Increased rates of bleeding with aspirin have been shown at the population level. And um, especially because you're over 70, people might argue that the risk of bleeding actually outweighs the possible benefits. Uh, again, extrapolating population data to the individual patient in front of you is the art of medicine. So I will leave that to you and your team, but I would say you have a couple of reasons why aspirin might be beneficial and age might be a reason not to do it. So that's my take on aspirin. All right. Paul, again, great question. In my opinion, get a CIMT for cardio risk. Yes, big out, big shout out for cardio risk. Cardio Risk reads all of my CIMTs. Big thanks to Todd and Heidi Eldridge, who are the uh dynamic duo who run that, and for uh Dr. Todd Eldridge in particular for making CIMT a reliable, repeatable test. I feel amazing about recommending for my patients. All right. How much radiation for a CTA? This is a very important question, and it is entirely dependent on the machine that you are getting your CTs done on. So there are newer, much more efficient scanners, and there are older scanners. The amount of radiation you're gonna get from a CT angiogram is really dependent on the scanner itself, and the newer ones are bringing radiation doses down, down, down. Uh, I am told that we can actually get approximately down to the level of a mammogram, even for a CT angio. That is certainly true for CAC, but even CT angio is getting that low. So I don't mean to minimize the impact of radiation, particularly if we're talking about procedures over time, right? So if you're somebody with high family risk, uh strong family history of premature events, and you are starting to get imaged in your 40s or your 30s, that's a lot of radiation if we're gonna extend this out years uh to try to monitor the effectiveness of therapy. And I think this is where CIMT and plaque detection by carotid ultrasound really shines. And CCTA is maybe something we do every five years, every 10 years. Uh, also, nobody knows exactly what the repeat frequency should be for CCTA. Uh CAC, people will say two to five years. Again, if you have not seen my video on why I don't recommend repeat CAC scores for people who've already had a positive one, uh, please go give that a watch because I think that explains a lot. But um, if you had a zero calcium score, when should you repeat it? Again, how old are you? Uh, how out of control are your general biomarkers and how strong is your family history? How soon do you want to know? I think anywhere in the two to five year range is probably reasonable to get a double zero score and use that. Is if you're testing at 35 and at 40, well, you're not done. That double zero does not give you the warranty forever. So it's probably a warranty for five to ten years. But uh after that, you probably need again repeat imaging if you're starting really young. All right. I think we are approaching the end of this. Let's see if I have any more. Yes, I have one more anonymous question, and then we are gonna start wrapping things up. But when is blood work done to check when you could, quote, have problems taking certain NEDs? So this person is asking about a torvostatin or coplitogril, which is Plavix, as an example. What happens behind the scenes in the lab to check what is going on? So this is everything from a very standard, let's check your liver enzymes to make sure that your medications have not pissed off your liver, to, you know, 30 to 50% of people might be resistant to Plavics and doing some specialized testing to understand if you are one of those people who might be resistant to the antiplatelet medicine, clopidogril or plavix. The lab testing thing is, you know, what's going on behind the scenes. Your doctor is trying to make a decision about what information do they need? What are the possible side effects of the medications? What are the chances that you need to be tested to see if you might have medication interactions or certain predispositions for that? And this is not terribly standardized. So what goes on behind the scenes is kind of a black box and really depends on who your physician is and what kind of information they are trying to get. There are some genetic tests that can be done to recognize whether you might be more likely to have problems or side effects with satins. I don't do them routinely in my practice, but if that's something you really want to know about, that is out there in the world. You could get it, but uh it's not terribly common. So what happens behind the scenes, it's really hard to predict. And then you're getting the labs back, and then you and your physician hopefully are going over that. Your doctor is interpreting those tests to decide: is there a problem? Is there a chance for an interaction here? Is there a chance this medicine isn't effective for you and we should go to a different one? All of that is possible, and um, that's what we do, right? Like that's what part of my day is spent doing is like ordering tests for my patients to figure out what information I need to get them the next step along in the process, and then getting those tests back and interpreting them, figuring out what we do next. All right. Can discuss gluten and leaky gut regarding glucose tolerance and plaque buildup. Andy Billy, that's an interesting question. I don't have a great answer about leaky gut, glucose tolerance or plaque buildup. That is um maybe something we could deep dive on another time. But off the top of my head, I don't have a study or any evidence that suggests that it's dramatic. But again, everybody's a little different. If you have poor glucose tolerance, that will definitely impact the risk for plaque buildup over time.

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Dr.

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JK, I'm 70 and just had my CIMT from cardiac. Arterial age of 52. Nice, nice. But 4.6 of plaque, only calcified plaque in right and left bulb. Hasn't changed in three years. Should I be concerned? So, you know, any plaque, of course, is a risk, but if it hasn't changed in three years, this is stable plaque. This is a dormant volcano. We hope that it will never create an issue for you, right? And what I tell patients who show up to my clinic is if this was all you ever had, four millimeters of plaque, and it never changes, you can die with this plaque, right? You can plaque is ultimately the best predictor I have of the enemy, but the enemy is stroke and heart attack and limb loss. The enemy is not truly by itself the plaque. It's just the best marker I have that talks to us about it. But um if it is calcified, if it has not changed and your arterial age is low, meaning your overall arterial inflammation is low, I don't think you're accumulating more plaque. There are a lot of people who wander around with calcium scores in the thousands with stable plaque who have modified their risk, dealt with their lifestyle, and gotten on program. And they will die with their calcium score in the thousands, hopefully at a very ripe old age in their sleep, you know, from who knows what. But my hope is that that is not something that will lead to significant disability, hospitalization, need for procedures. That is what I am trying to help people avoid. And, you know, what else are we going to do about it, right? If your risk is optimal, your arterial age is low, and you're continuing to check it, it sounds like you're on program. It sounds like you are doing the right things. And I hope that that means it will never cause you any trouble. Is choline good for neurologic damage caused by a stroke? I don't know the answer to that off the top of my head. Uh I don't, but it's a great question. We'll look into it. And I think we are gonna wrap it here today, guys. You have been an amazing, amazing group. Thank you so much for coming out. This has been a lot of fun. I hope I got to most, or if not all, of the questions. You guys have been amazing. Until next time, guys, I hope you take really good care.